Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients.
2018
Authors:
Paunović, VericaVukovič Petrović, Irena
Milenković, Marina
Janjetović, Kristina
Pravica, Vera
Dujmović, Irena
Milošević, Emina
Martinović, Vanja
Mesaroš, Šarlota
Drulović, Jelena
Trajković, Vladimir
Document Type:
Article (Published version)
,
© 2018 Elsevier B.V.
Metadata
Show full item recordAbstract:
Autophagy, a process of controlled self-digestion which regulates cell homeostasis, is involved in innate and adaptive immunity. We investigated the expression of autophagy genes and autophagic activity in distinct lymphocyte populations in treatment-naive MS patients. The mRNA and protein levels of autophagy-related (ATG)5, required for autophagosome formation, were increased in CD4+and CD4-T cells, but not B cells of MS patients compared to control subjects. The expression of other investigated autophagy genes, as well as the autophagic activity, did not significantly differ between the two groups. ATG5 mRNA levels in CD4+T cells from MS patients were positively correlated with those of the proinflammatory cytokine tumor necrosis factor. These data suggest that autophagy-independent increase in ATG5 expression might be associated with the proinflammatory capacity of T cells in multiple sclerosis.
Keywords:
ATG5; Autophagy; LC3; Multiple sclerosis; SQSTM1; T cells; TNFSource:
Journal of Neuroimmunology, 2018, 319, 100-105Funding / projects:
- Modulation of intracellular energy balance-controlling signalling pathways in therapy of cancer and neuro-immuno-endocrine disorders (RS-MESTD-Integrated and Interdisciplinary Research (IIR or III)-41025)
- Immunopathogenic and regulatory mechanisms in autoimmune diseases and chronic inflamation (RS-MESTD-Basic Research (BR or ON)-175038)
- Comparative analysis of clinical features and biomarkers to predict disease evolution in multiple sclerosis and other immune-mediated neurological disorders (RS-MESTD-Basic Research (BR or ON)-175031)
DOI: 10.1016/j.jneuroim.2018.03.001
ISSN: 0165-5728
PubMed: 29548704
WoS: 000433016400014
Scopus: 2-s2.0-85043451518
URI
http://www.jni-journal.com/article/S0165-5728(17)30538-6/abstracthttps://radar.ibiss.bg.ac.rs/handle/123456789/3014